ArticleInternational journal of cancer2013
Epstein-Barr virus-induced epigenetic alterations following transient infection.
Article in International journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- EBV-Induced LINC00944: A Driver of Oral Cancer Progression and Influencer of Macrophage Differentiation.Cancers · 2025Article
- The Oncogenic Role ofInternational journal of molecular sciences · 2024Article
- Epstein-Barr virus LMP1 protein promotes proliferation and inhibits differentiation of epithelial cells via activation of YAP and TAZ.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- New insight into Epstein-Barr virus infection using models of stratified epithelium.PLoS pathogens · 2023Article
- Review
- EBV persistence in gastric cancer cases conventionally classified as EBER-ISH negative.Infectious agents and cancer · 2022Article
- Article
- Could Changing the DNA Methylation Landscape Promote the Destruction of Epstein-Barr Virus-Associated Cancers?Frontiers in cellular and infection microbiology · 2021Review
- Article
- Review
- Extranodal NK/T-cell lymphoma, nasal type without evidence of EBV infection.Oncology letters · 2020Article
- Multi-layered control of PD-L1 expression in Epstein-Barr virus-associated gastric cancer.Journal of cancer metastasis and treatment · 2020Article
- Overexpression of Epstein-Barr virus-encoded latent membrane protein-1 (LMP-1) in oral squamous cell carcinoma.BMC oral health · 2019Article
- Inhibition of Epstein-Barr Virus Replication in Human Papillomavirus-Immortalized Keratinocytes.Journal of virology · 2019Article
- Molecular features and translational outlook for Epstein-Barr virus-associated gastric cancer.Future virology · 2018Article
- Article
- Epstein-Barr virus in the pathogenesis of oral cancers.Oral diseases · 2018Review
- Epstein-Barr virus stably confers an invasive phenotype to epithelial cells through reprogramming of the WNT pathway.Oncotarget · 2018Article
- Epstein-Barr virus infection and nasopharyngeal carcinoma.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Epstein-Barr virus-associated lymphomas.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Epstein-Barr virus (EBV) is a known tumor virus associated with an increasing array of malignancies; however, the association of the virus with certain malignancies is often erratic. To determine EBV's contributions to tumorigenesis in a setting of incomplete association, a transient model of infection was established where a clonal CCL185 carcinoma cell line infected with recombinant EBV was allowed to lose viral genomes by withdrawal of selection pressure. Global gene expression comparing EBV-negative, transiently infected clones to uninfected controls identified expression changes in more than 1,000 genes. Among downregulated genes, several genes known to be deoxyribonucleic acid (DNA) methylated in cancer were identified including E-cadherin and PYCARD. A cadherin switch, increased motility and enhanced cellular invasiveness present in EBV-positive cells were retained after viral loss, indicating an epigenetic effect. Repression of PYCARD expression was a result of increased promoter CpG methylation, whereas loss of E-cadherin expression after transient EBV infection did not correlate with increased DNA methylation of the E-cadherin promoter. Rather, repression of E-cadherin was consistent with the formation of a repressive chromatin state. Decreased histone 3 or 4 acetylation at the promoter and 5' end of the E-cadherin gene was observed in an EBV-negative, transiently infected clone relative to the uninfected controls. These results suggest that EBV can stably alter gene expression in a heritable fashion in formerly infected cells, whereas its own contribution to the oncogenic process is masked.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.